ArticleOncogene2004
Loss of the INI1 tumor suppressor does not impair the expression of multiple BRG1-dependent genes or the assembly of SWI/SNF enzymes.
Article in Oncogene, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
39 citing papers in PubMed, 78 citations in OpenAlex.
- SWI/SNF Chromatin Remodelling Complex in Hepatic Physiology: Mechanistic Insights Into Development, Homeostasis and Pathogenesis.Journal of cellular and molecular medicine · 2026Review
- BRG1 establishes the neuroectodermal chromatin landscape to restrict dorsal cell fates.Science advances · 2024Article
- Review
- Global Chromatin Changes Resulting from Single-Gene Inactivation-The Role of SMARCB1 in Malignant Rhabdoid Tumor.Cancers · 2021Article
- The BAF complex in development and disease.Epigenetics & chromatin · 2019Review
- Disruption of mammalian SWI/SNF and polycomb complexes in human sarcomas: mechanisms and therapeutic opportunities.The Journal of pathology · 2018Review
- SMARCB1 is required for widespread BAF complex-mediated activation of enhancers and bivalent promoters.Nature genetics · 2017Article
- Loss of Snf5 Induces Formation of an Aberrant SWI/SNF Complex.Cell reports · 2017Article
- SMARCB1-mediated SWI/SNF complex function is essential for enhancer regulation.Nature genetics · 2017Article
- The molecular pathogenesis of schwannomatosis, a paradigm for the co-involvement of multiple tumour suppressor genes in tumorigenesis.Human genetics · 2017Review
- Evaluation of the role of downregulation of SNF5/INI1 core subunit of SWI/SNF complex in clear cell renal cell carcinoma development.American journal of cancer research · 2017Article
- Chromatin Remodeler Recruitment during Macrophage Differentiation Facilitates Transcription Factor Binding to Enhancers in Mature Cells.The Journal of biological chemistry · 2016Article
- Review
- SMARCA4 inactivation defines a group of undifferentiated thoracic malignancies transcriptionally related to BAF-deficient sarcomas.Nature genetics · 2015Article
- SNF5/INI1 deficiency redefines chromatin remodeling complex composition during tumor development.Molecular cancer research : MCR · 2014Article
- Vulnerabilities of mutant SWI/SNF complexes in cancer.Cancer cell · 2014Review
- Mechanisms by which SMARCB1 loss drives rhabdoid tumor growth.Cancer genetics · 2014Review
- A rationale to target the SWI/SNF complex for cancer therapy.Trends in genetics : TIG · 2014Review
- SNF5 is an essential executor of epigenetic regulation during differentiation.PLoS genetics · 2013Article
- Functional redundancy of SWI/SNF catalytic subunits in maintaining vascular endothelial cells in the adult heart.Circulation research · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
The INI1/hSNF5 tumor suppressor is an integral component of mammalian SWI/SNF chromatin remodeling enzymes that contain SNF2 family ATPases BRM (Brahma) or BRG1 (Brahma Related Gene 1) and that contribute to the regulation of many genes. Genetic studies of yeast SWI/SNF enzyme revealed similar phenotypes when single or multiple components of the enzyme were deleted, indicating a requirement for each subunit. To address the contribution of INI1 in the regulation of SWI/SNF-dependent genes in mammalian cells, we examined the expression of multiple BRG1-dependent, constitutively expressed genes in INI1-deficient cancer cell lines. At least one INI1-deficient line expressed each gene, and reintroduction of INI1 had negligible effects on expression levels. Lack of INI1 also did not prevent interferon gamma (IFNgamma)-mediated induction of CIITA, which is BRG1 dependent, and GBP-1, which is BRG1 enhanced, and reintroduction of INI1 had minimal effects. Chromatin immunoprecipitation experiments revealed that BRG1 inducibly binds to the CIITA promoter despite the absence of INI1. Unlike yeast deleted for the INI1 homologue, SWI/SNF enzymes in INI1-deficient cells were largely intact. Thus in human cells, SWI/SNF enzyme complex formation and the expression of many BRG1-dependent genes are independent of INI1.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.